ArticleRenal failure2025
Origin of poorly galactosylated IgA1 other than mucosa: a viewpoint from a report on patient with IgA vasculitis.
Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Patients presenting monoclonal gammopathy of renal significance (MGRS) and IgA vasculitis collectively have rarely been reported. This study reports one patient with monoclonal IgA and λ, and with IgA positive-mesangial proliferative glomerulonephritis. The patient manifested slight chronic nephritic syndrome, and his serums tested positive for M protein (monoclonal IgA and λ). As a result of bone wear, the plasma cell ratio of these patients was confirmed to be mildly increased in peripheral blood smears. Just like typical IgA nephropathy or IgA vasculitis patients, serum poorly galactosylated IgA1 antibodies were found in the patient compared to the controls. The patient was diagnosed with mild mesangial proliferative IgA vasculitis based on renal biopsy. Besides, immunofluorescence/immunohistochemistry confirmed immune deposits predominantly containing galactose-deficient IgA1 (GD-IgA1) and λ in the glomerular mesangium and the walls of the skin's blood vessels. The pathological findings support the hypothesis that monoclonal IgA, which originate from bone marrow plasma cells, rather than mucosally primed B cells, also may be galactose deficient. This may be a new pathological source of IgA-proliferative glomerulonephritis.
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